Glyceraldehydes-derived Advanced Glycation End Products Decrease White Adipose Tissue Weight and Downregulate Leptin, Adiponectin, and Macrophage Marker

2010 ◽  
pp. 51-57
Keyword(s):  
Adipose Tissue ◽  
Advanced Glycation End Products ◽  
White Adipose Tissue ◽  
Advanced Glycation ◽  
Tissue Weight ◽  
Macrophage Marker ◽  
Adipose Tissue Weight ◽  
Glycation End Products ◽  
End Products

In vitro chronic glycation induces AGEs accumulation reducing insulin stimulated glucose uptake and increasing GLP1R in adipocytes

2021 ◽  
Author(s):  
Nino C Chilelli ◽  
Alessia Faggian ◽  
Francesca Favaretto ◽  
Gabriella Milan ◽  
Chiara Compagnin ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Uptake ◽  
Advanced Glycation End Products ◽  
Glucose Transporter ◽  
Adipogenic Differentiation ◽  
Continuous Process ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Insulin Responsiveness

Glycation is one of the most important post-translational modifications in cells and tissues and gives rise to highly reactive species called advanced glycation end products (AGEs). AGEs exert their pathological effects through different ways and previous reports suggest that they may also affect adipose tissue function and insulin sensitivity. All the data belong only to short-term treatments; however, in vivo glycation is a continuous process. To fill this gap, our study investigated the effect of chronic pro-glycating conditions on adipogenesis and adipocyte's insulin responsiveness. Our results show that chronic pro-glycating treatments with methylglyoxal (MGO) and MGO modified-BSA (BSA-MGO) do not display cytotoxicity but modify gene expression without affect adipogenic differentiation. These treatments induce different levels of intracellular accumulation of AGEs which colocalize with the insulin-sensitive glucose transporter GLUT4 (solute carrier family 2 member 4- SLC2A4) in the cytoplasm; in particular, BSA-MGO reduces glucose uptake. Moreover, the adipocytes differentiated in pro-glycating conditions display an enhancement in the protein expression of the receptor for advanced glycation end products (RAGE) and glucagon-like peptide 1 receptor (GLP1R). These results suggest that intracellular AGEs could link alterations in GLP1 signaling and insulin resistance in adipose tissue, revealing that GLUT4 protein can be susceptible to glycation. Further studies are needed to clarify if this pathway could be targeted and if the reduction of AGEs accumulation in adipocytes can ameliorate insulin responsiveness.

scholarly journals Expression of the Receptor for Advanced Glycation End Products in Epicardial Fat: Link with Tissue Thickness and Local Insulin Resistance in Coronary Artery Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Elena Dozio ◽  
Elena Vianello ◽  
Silvia Briganti ◽  
John Lamont ◽  
Lorenza Tacchini ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Adipose Tissue ◽  
Coronary Artery ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Impaired Insulin ◽  
Artery Disease ◽  
Rage Expression

Increased expression of receptor for advanced glycation end products (RAGE) in adipose tissue has been associated with inflammation, adipocyte hypertrophy, and impaired insulin signal. Epicardial adipose tissue (EAT), a visceral fat surrounding the myocardium, is potentially involved in the onset/progression of coronary artery disease (CAD). To date, the role of RAGE in EAT has not been explored much. We examined whether the RAGE expression in EAT was associated with EAT adiposity and metabolic dysfunctions normally found in CAD patients. EAT samples were obtained from 33 patients undergoing open-heart surgery. EAT expression of RAGE, GLUT4, adiponenctin, GLO1, HMGB1, TLR-4, and MyD88 was analyzed by microarray. EAT thickness was quantified by echocardiography. Anthropometric measures and clinical parameters were taken. BMI, HOMA-IR, and LAP indices were calculated. With increasing RAGE expression in EAT we observed increases in EAT thickness, reduced expression of GLUT4, adiponectin, and GLO1, and elevations of HMGB1, TLR-4, and MyD88. There were significant correlations between RAGE and EAT thickness and between RAGE and the genes. LAP was higher in patients with increased RAGE expression. Our data suggest that in CAD patients RAGE may be involved in promoting EAT adiposity and metabolic dysfunction, such as impaired insulin signaling.

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